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Legumes and a few other plant species can establish a symbiotic relationship with nitrogen-fixing rhizobia, which enables them to survive in a nitrogen-deficient environment. During the course of nodulation, infection with rhizobia induces the dedifferentiation of host cells to form primordia of a symbiotic organ, the nodule, which prepares plants to accommodate rhizobia in host cells. While these nodulation processes are known to be genetically controlled by both plants and rhizobia, recent advances in studies on two model legumes, Lotus japonicus and Medicago truncatula, have provided great insight into the underlying plant-side molecular mechanism. In this chapter, we review such knowledge, with particular emphasis on two key processes of nodulation, nodule development and rhizobial invasion.
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http://dx.doi.org/10.1016/bs.ircmb.2015.01.004 | DOI Listing |
Curr Opin Virol
September 2025
Department of Hematology, Rheumatology and Infectious Diseases, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan. Electronic address:
Human T-cell leukemia virus type I (HTLV-1) was the first human pathogenic retrovirus to be discovered. HTLV-1 induces a T-cell malignancy, adult T-cell leukemia-lymphoma (ATL), and inflammatory diseases, such as HTLV-1-associated myelopathy (HAM), HTLV-1 uveitis (HU), and HTLV-1-associated pulmonary disease (HAPD). Importantly, HTLV-1 maintains persistent infection by regulating viral gene expression and disrupting host signaling pathways - activities that are closely linked to its pathogenicity.
View Article and Find Full Text PDFMol Ther
September 2025
Be Biopharma, Cambridge, MA, 02139, USA. Electronic address:
Hemophilia B gene therapy treatments currently have not addressed the need for predictable, durable, active, and redosable factor IX (FIX). Unlike conventional gene therapy, engineered B Cell Medicines (BCMs) are durable, redosable, and titratable, and thus have the potential to address significant unmet needs in the Hemophilia B treatment paradigm. BE-101 is an autologous BCM comprised of expanded and differentiated B lymphocyte lineage cells genetically engineered ex vivo to secrete FIX-Padua.
View Article and Find Full Text PDFBull Cancer
September 2025
Service d'hématologie, département d'oncologie, hôpitaux universitaire de Genève (HUG), faculté de médecine, université de Genève, Genève, Suisse. Electronic address:
Acute graft-versus-host disease (GVHDa) is one of the leading causes of morbidity and mortality after allogeneic hematopoietic stem cell transplant (HSCT) patients. While the first-line consensus treatment has been based on systemic corticosteroid therapy for many years, ruxolitinib has recently been approved and has become the standard second-line treatment. Nevertheless, the effectiveness of ruxolitinib remains limited to 40 % of cortico-resistant patients, raising the crucial question of selecting a third-line treatment.
View Article and Find Full Text PDFMicrobes Infect
September 2025
Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530007, P.R. China. Electronic address:
Background: While autophagy is pivotal in antimicrobial defense, its regulatory role in Talaromyces marneffei (TM) infected bronchial epithelium remains elusive.
Objective: To elucidate the impact of TM infection on autophagy in bronchial epithelial cells and to identify the key molecular regulators involved in this process.
Methods: Primary computational screening identified core autophagy modulators.
Cell
September 2025
Department of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. Electronic address:
Adaptation of intestinal helminths to vertebrates involved the evolution of strategies to attenuate host tissue damage to support parasite reproduction and dissemination of offspring to the environment. Helminths initiate the IL-25-mediated tuft cell-type 2 innate lymphoid cell (ILC2) circuit that enhances barrier protection of the host, although viable parasites can target and limit this pathway. We used IL-25 alone to create small intestinal adaptation, marked by anatomic and immunologic changes that persisted months after induction.
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